Apoptosis pathways are impaired in fibroblasts from patients with SSc, leading to chronic fibrosis. Nonetheless, PUMA/p53 pathway may not be involved in dysfunction of apoptosis mechanisms in fibroblasts of patients with SSc.

PUMA promotes the cytosolic release of mitochondrial DNA and activation of the DNA sensors DAI/Zbp1 and STING, leading to enhanced RIP3 and MLKL phosphorylation in a positive feedback loop.

ERK1/2/p53/PUMA signaling axis is related to cisplatin-induced cell death in ovarian cancer cells.

these results establish a critical role of PUMA in mediating the anticancer effects of deguelin in lung cancer cells and provide the rationale for clinical evaluation.

AGG is also found to trigger ubiquitination of PUMA which in turn interacted with p62 for prompting mitophagy suggesting that AGG turns on PUMA-mediated mitophagy in U87MG cells in both p62-dependent as well as in p62-independent manner

Low PUMA expression is associated with cancer.

Authors show that blockade of cAMP signaling using MDL12330A led to an increase in PUMA transcript levels, but not p21 in melanoma cells. Results suggest that transcriptional repression is one of the functions of the cAMP-Epac signaling pathway.

Altogether, these findings suggest that in normal/high glucose condition a mutual unbalance between p53-dependent apoptosis (PUMA) and autophagy (DRAM) gene occurred, modifying the ADR-induced cancer cell death in HG both in vitro and in vivo.

Knockdown of Slug enhanced the antitumor activity of DOX in SW1736 cells via induction of PUMA upregulation. Our results suggest that targeting of Slug has good potential for the development of new therapeutic strategies for Anaplastic thyroid carcinoma.

Mouse (Murine) BCL2 Binding Component 3 (BBC3) Interaktionspartner

The study suggests that targeting MIAT may protect against cardiomyocytes against hypoxia-reperfusion injury or myocardial ischemia-reperfusion injury via inhibition of cell apoptosis, mediated by NF-kappaB and PUMA signaling pathway.

TFEB functions cell-autonomously through PUMA induction and Bax-Bak activation to promote programmed cell death of a subset of premyelinating oligodendrocytes, allowing selective elimination of oligodendrocytes in normally unmyelinated brain regions.

Using gain- and loss-of-function approaches, we identified a unique role of miR-143/PUMA in mediating microglial activation via regulation of NLRP3 inflammasome activation.

PUMA promotes the cytosolic release of mitochondrial DNA and activation of the DNA sensors DAI/Zbp1 and STING, leading to enhanced RIP3 and MLKL phosphorylation in a positive feedback loop.

Expression from a luciferase reporter construct containing the 2 kb fragment of the promoter region of bcl-2-binding component 3 (PUMA) is enhanced by activation of the muscle regulatory transcription factor MyoD in both myoblasts and fibroblasts and diminishes by silencing of MyoD in myoblasts. E-Box Sequences at position - 857 of PUMA is the binding site for MyoD.

Proapoptotic proteins BIM and PUMA are not critical for the reticulocyte apoptosis caused by loss of the pro-survival protein BCL-XL.

The mitochondrial apoptotic pathway, activated by BH3-only proteins, BIM and PUMA, is essential for endoplasmic reticulum stress-induced cell death; DR5 as well as caspase-8 are not required for this process.

Mir143-BBC3 has roles in microglial survival in the context of drug abuse

In the mouse model of silicosis, Bbc3 knockout mice clearly exhibited decreased levels of autophagy and fibrosis progression. These results suggest that downregulation of BBC3 expression may become a novel therapeutic strategy for the treatment of silicosis.

Data show that Emu-Myc mice lacking both p21 and PUMA developed lymphoma at a rate considerably longer latency than Emu-Myc;p53(+/-)mice.

Our data show a novel pathway of infection-induced apoptosis that enhances our understanding of the mechanism by which BH3-only proteins control apoptotic host cell death during Listeria infection.

Overexpression of miR-29 or miR-24 is sufficient to inhibit the induction of Bim and Puma in young sympathetic neurons.

loss of PUMA had no impact on the loss of platelets caused by loss of BCL-XL. It therefore remains to be established whether other BH3-only proteins play a critical role in induction of apoptosis in platelets or whether their death is controlled solely by the interactions between BCL-XL with BAK and BAX.

PUMA is dispensable for glucose homeostasis in lean and obese mice, but it can affect leptin levels and food intake during obesity.

MYSM1 is a critical negative regulator of p53 transcriptional programs in hematopoiesis, and its repression of Bbc3/PUMA expression is essential for multipotent progenitor survival, and partly contributes to maintaining hematopoietic stem cel function.

Therapeutic response to non-genotoxic activation of p53 by Nutlin3a is driven by PUMA-mediated apoptosis in lymphoma cells.

Bim and Puma overlapped apoptosis only partially during physiological apoptotic stage and they were present in non-apoptotic parts of the follicles.

BBC3 Antigen-Profil

Beschreibung des Gens

This gene encodes a member of the BCL-2 family of proteins. This family member belongs to the BH3-only pro-apoptotic subclass. The protein cooperates with direct activator proteins to induce mitochondrial outer membrane permeabilization and apoptosis. It can bind to anti-apoptotic Bcl-2 family members to induce mitochondrial dysfunction and caspase activation. Because of its pro-apoptotic role, this gene is a potential drug target for cancer therapy and for tissue injury. Alternative splicing results in multiple transcript variants.